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Pathology > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

what is haemostasis

A

response to vessel injury and bleeding by causing bleeding to stop, meaning to keep blood within a damaged blood vessel

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2
Q

what is essential in haemostasis

A
  • for the blood to be kept moving
  • platelets
  • coagulation factors
  • anticoagulant factors
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3
Q

outline clot formation

A

platelets aggregate and stick to the wall forming a clot.
- this activates coagulation causing the activation of thrombin to change fibrinogen into fibrin which strengthens the platelet clod

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4
Q

what is fibrinolysis

A

the break down of the clot into fibrin fragements

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5
Q

what and where are platelets produced

A

by megakaryocytes which bud of from the cytoplasm in bone marrow

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6
Q

what is the normal platelet count

A

150-400

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7
Q

what is the normal life span of a platelet

A

7-10 days

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8
Q

what do platelets do

A

adhere to the exposed collagen on the damaged vessel wall via vWF

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9
Q

what activates platelets

A

ADP, thromboxane and other substances

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10
Q

name some factors which mediate platelet aggregation

A

fibrinogen, collagen , ADP, thromboxane

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11
Q

what converts fibrinogen to fibrin

A

thrombin

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12
Q

where are coagulation factors produced

A

in the liver

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13
Q

name some natural anticoagulants

A

Protein C. Protein S. antithrombin

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14
Q

what are the 2 pathways in blood clotting

A

intrinsic (damaged surface) and extrinsic (trauma)

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15
Q

which factors do both pathways of the blood clotting cascade cause the production of

A

V, X, prothrombin and fibrinogen

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16
Q

what factor is involved in the extrinsic pathway

A

VII

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17
Q

what factors are involved in the intrinsic pathway

A

VIII, IX, XI, XII

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18
Q

what is tissue factor

A

receptor for factor VII (extrinsic pathway) which activates the cascade

19
Q

what clotting factor is the start pf the common pathway

A

X

20
Q

what is thrombin burst

A

when in the extrinsic pathway, circulating thrombin comes into contact with the tissue factor receptors which causes more thrombin to be recruited

21
Q

what is the von Willebrand factor

A

a glycoprotein involved in platelet adhesion to the vessel wall, platelet aggregation and also stabilised FVIII

22
Q

what initiates activation of clotting factors

A

exposure of collagen and tissue factor

23
Q

what is the fibrin clot broken down into

A

D-dimers (small protein fragments)

24
Q

what is thrombophilia

A

where the blood clots too much - this is prevented by anticoagulants

25
Q

name 2 congenital coagulation factor disorders

A 
Haemophilia A (factor 8 deficiency)
Haemophilia B (factor 9)
26
Q

name 3 acquired coagulation factor disorders

A 
Liver disease (reduction production of protein coagulation factors)
Vit K deficiency 
Warfarin (inhibit Vit K)
27
Q

what do coagulation factor disorders cause

A 
muscle haematomas (collection of blood outside a vessel)
recurrent haemarthroses (bleeding into a joint)
joint deformity 
prolonged bleeding following operation,dental extraction
intracerebral haemorrhage
28
Q

what inheritance pattern in Haemophilia A

A

autosomal recessive

29
Q

what is used to treat haemophilia A

A

recombinant factor VIII

30
Q

what is Von Willebrands disease

A

an autosomal dominant disease where there is abnoral platelet adhesion to vessel wall and a reduced activity of factor VI due to reduction in vWF

31
Q

what is seen in Von Willebrands disease

A
  • easy bruising, epistaxis, gum bleeding, prolonged bleeding after trauma or surgery
32
Q

what congenital vessel wall conditions are there

A
  • hereditary haemorrhagic telangiectasia (where arteries join directly to veins)
  • Ehlers Danlos
33
Q

name 4 causes of acquired vessel wall conditions

A
  • purpura
  • steroids
  • infection
  • vit C deficiency (collagen needed for platelet clot)
34
Q

what is seen in vessel wall abnormalities

A

easy bruising, spontaneous bleeding from vessel mainly affecting skin and mucus membranes

35
Q

what is a reduction in platelets called

A

thrombocyopenia

36
Q

what causes a low platelet count

A
  • reduced production

- increased removal

37
Q

what causes n increased removal of platelets

A
  • non-immune destruction
  • immune destruction
  • splenic pooling
38
Q

give an example of a type of immune destruction of platelets

A

immune thrombocytopenic purpura

  • produces autoatibodies against factor clotting factors
  • treated with immunosuppressants
  • cant have platelet transfusion
39
Q

give an exmaple of a type of non immune destruction of platelets

A

DIC

40
Q

why may there be a reduced production of platelets

A
  • B12/folate deficiency
  • infiltration of bone marrow by cancer cells or fibrosis
  • drugs
  • viruses
41
Q

what are the consequences of thrombocytopenia

A
  • asymptomatic until platelet count is below 30
  • easy bruising
  • petechiae which develop into purpura
  • mucosal bleeding
  • severe bleeding after trauma
42
Q

give an example of an hereditary platelet function disorder

A

Bernard Soulier (impaired platelet granule content)

43
Q

give an example of an acquired platelet function disorder

A
  • aspirin

- uraemia (renal failure)

44
Q

what is DIC

A

Disseminated Intravascular Coagulopathy
widespread activation of the clotting cascade that results in the formation of blood clots in the small blood vessels throughout the body. This leads to compromise of tissue blood flow and can ultimately lead to multiple organ damage. In addition, as the coagulation process consumes clotting factors and platelets, normal clotting is disrupted and severe bleeding can occur from various sites.

Pathology (13 decks)

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